The purpose of this study was to determine whether chronic, low-level
exposure of mammary-tumor-prone mice to 2450 MHz radiofrequency radiat
ion (RFR) promotes an earlier onset (decreased latency), a greater tot
al incidence, or a faster growth rate of mammary tumors. One hundred C
3H/HeJ mice were exposed in circularly polarized waveguides (CWG) for
18 months (20 h/day, 7 days/wk) to continuous-wave, 2450 MHz RFR at a
whole body average specific absorption rate (SAR) of 0.3 W/kg; 100 mic
e were sham exposed. Before exposure, SARs were determined calorimetri
cally; during experimentation, SARs were monitored by differential pow
er measurement. All animals were visually inspected twice daily and we
re removed from the CWG cages for a weekly inspection, palpation, and
weighing. From the time of detection, tumor size was measured weekly.
Animals that died spontaneously, became moribund, or mere killed after
18 months of exposure were completely necropsied; tissues were fixed
and subjected to histopathological evaluations. Results showed no sign
ificant difference in weight profiles between sham-irradiated and irra
diated mice. Concerning mammary carcinomas, there was no significant d
ifference between groups with respect to palpated tumor incidence (sha
m = 52%; irradiated = 44%), latency to tumor onset (sham = 62.3 +/- 1.
2 wk; irradiated = 64.0 +/- 1.6 wk), and rate of tumor growth. In gene
ral, histopathological examination revealed no significant differences
in numbers of malignant, metastatic, or benign neoplasms between the
two groups; a significantly greater incidence of alveolar-bronchiolar
adenoma in the sham-irradiated mice was the only exception. In additio
n, survival analysis showed no significant difference in cumulative pe
rcent survival between sham and irradiated animals. Thus, results indi
cate that under the conditions of this study, long-term, tow-level exp
osure of mammary-tumor-prone mice to 2450 MHz RFR did not affect mamma
ry tumor incidence, latency to tumor onset, tumor growth rate, or anim
al longevity when compared with sham-irradiated controls. (C) 1998 Wil
ey-Liss, Inc.